Abstract

It has been generally accepted by cardiac electrophysiologists that the diastolic (resting) membrane potential, ED, of myocardial cells is determined, primarily, by the potassium equilibrium potential, EK (2). This has been shown to be true for myocardial cells in which intracellular potassium activity, ai(K), has been measured with potassium selective microelectrodes (4, 8). McDonald and MacLeod, however, published experimental results (5), which they later expanded (6), from which they concluded that under some conditions ED is not primarily determined by EK. They superfused guinea pig papillary muscles under nitrogen and found there was a large loss of intracellular potassium but ED did not increase as much as EK, i.e. ED became negative with respect to EK.. They concluded that during hypoxia, ED was maintained negative with respect to EK. by electrogenic sodium pumping. Bosteels et al. (2) did similar experiments with embryonic chick heart and found, to the contrary, that ED always remained positive with respect to EK. We have repeated the experiments with guinea pig papillary muscles using potassium selective electrodes, instead of whole tissue analysis, to measure intracellular potassium.

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